The mechanism by which infected rats focus their cellular defenses at sites of microbial invasion would be analyzed from the standpoint of the number and types of lymphocytes which localize in inflammatory foci, the fate of the cells after leaving the blood and their capacity to interact with macrophages in various ways. Labeling procedures would be used to trace the tissue disposition of defined lymphocyte subsets after intravenous transfer into syngeneic recipients. Prominence would be given to the elucidation of control mechanisms regulating the production of effector T cells, forces influencing localization of these cells at sites of bacterial implantation and the mechanism whereby they promote the local accumulation and activation of monocyte-derived macrophages. Among the questions to be asked are whether products of antigen-stimulated lymphocytes, particularly macrophage migration inhibitory factor (MIF) and chemotactic factors, influence the structuring of lesions? Here an effort would be made to correlate local release of MIF and chemotactic factors with extravasation and local accumulation in exudates of radioactively labeled macrophages. Techniques developed in earler studies of the inflammation induced by listeria monocytogenes would be carried forward in an effort to define cell traffic patterns and immunological events associated with the development of chronic inflammatory exudates and granulomata induced by BCG.